期刊文献+

高原低氧诱导细胞应激试验研究 被引量:4

High altitude hypoxia-induced cell stress
原文传递
导出
摘要 目的:探讨高原低氧状态对诱导实验鼠细胞应激性的作用和影响。方法:设定A,B,C 3组,分别再将其分为实验组(A1,B1,C1)和对照组(A2,B2,C2),每小组18只,共108只实验鼠,雌雄各半,A组和C组用CR小鼠,B组用Wistar大鼠,A1组分析快速进入海拔3 820 m的缺氧诱导因子-1α表达特点;B1组置于400-420 kPa低压氧舱内压下,观察不同低氧暴露时间对大鼠心肌线粒体的影响;C组分析对比在不同海拔高度、不同氧浓度、不同天数的血浆血管内皮生长因子表达水平。对照组在海拔800 m进行实验。结果:A1组内皮素-1α的浓度逐渐上升,小鼠心肌细胞缺氧诱导因子-1α实验A1组阳性显著高于A2组;B组随进入低氧环境的天数延长,大鼠心肌线粒体的数量发生不同改变;C1组血管内皮生长因子浓度随天数增加而增加,与C2组比较差异有统计学意义。结论:低氧低压环境条件可促进实验鼠心肌细胞缺氧诱导因子-1α表达,实验鼠有低氧适应(习服)过程,血管内皮生长因子调控与氧含量相关,随氧含量下降而表达上升。 Objective To discuss the influence of high altitude hypoxia on stress in induced mouse cells.Methods A total of 108 mice(male and female in half) were divided into A,B and C groups,which were subdivided into A1,B1,C1 groups(experimental group) and A2,B2,C2 groups(control group).Group A and C used CR mice,and group B used Wistar rats.Group A1 was quickly accessed to an altitude of 3 820 meters for hypoxia-inducible factor-1α expression analysis.Group B1 was placed in 400 to 420 kPa low-pressure oxygen chamber to observe the effects of different hypoxia exposure time on rat heart mitochondria.Group C was analyzed and compared the plasma levels of vascular endothelial growth factor expression at different altitudes,different oxygen concentrations and different days.Control group was experimented at an altitude of 800 meters.Results The endothelin-1α concentration gradually increased in group A1,and hypoxia-inducible factor-1α of myocardial cells in group A1 was significantly higher than that in group A2.The number of myocardial mitochondria in group B changed with the period in low oxygen condition.The three different concentrations of vascular endothelial growth factor increased with the number of days increased in group C1,which showed a significant difference compared with group C2.Conclusion Low oxygen conditions can promote the expression of hypoxia-inducible factor-1α in myocardial cells.The mice with hypoxia prompt adaptation(acclimatization) process.The regulation of vascular endothelial growth factor is related with the oxygen content,and increases in the expression with the decline in oxygen content.
出处 《中华实用诊断与治疗杂志》 2010年第6期566-568,共3页 Journal of Chinese Practical Diagnosis and Therapy
基金 国家"十一五"863课题(2006AA020905)
关键词 细胞应激 缺氧诱导因子 转录因子 血管内皮生长因子 线粒体 Cell stress hypoxia-inducible factor transcription factor vascular endothelial growth factor mitochondria
  • 相关文献

参考文献10

  • 1马芳芳,沈晓丽,林立芳,韩莉莉.缺氧诱导因子-1对心肌细胞缺氧/复氧损伤的保护作用[J].中华实用诊断与治疗杂志,2009,23(3):223-226. 被引量:9
  • 2Kultz D. Molecular and evolutionary basis of the cellular stress response[J]. Annu Rev Physiol,2005,67(11):225-257.
  • 3Ferrara N. Molecular and biological properties of vascular endothelial growth factor[J]. J Mol Med,1999,77(7):527-543.
  • 4Kang P M, Haunstetter A, Aoki H, et al. Morphological and molecular characterization of adult cardiomyocyte apoptosis during hypoxia and reoxygenation[J]. Circ Res, 2000,87(2): 118-125.
  • 5Pugh C W, Ratclife P J. Regulation of angiogenesis by hypoxia: roieofthe HIFsystem[J]. Nat Med,2003,9(6):677-684.
  • 6Lynn E G, Lu Z, Minerbi D, et al. The regulation control and consequences of mitochondrial oxygen utilization and disposition in the heart and skeletal muscle during hypoxia[J]. Antioxid Redox Signal,2007,9(9) :1353-1357.
  • 7Cummins E P, Taylor C T. Hypoxia responsive transcription factors[J]. Pflugers Arch,2005,450(6) :363-371.
  • 8Date T, Mochizuki S, BeIanger A J, et al. Expression of constitutively stable hybrid hypoxia inducible factor-1alpha protects cultured rat cardiomyocytes against simulated ischemia reperfusion injury [J]. Am J Physiol Cell Physiol, 2005,288(2): C314-320.
  • 9胡娟,胡媛姮,李青,马建,邓贵福.缺氧损害对锌指蛋白A20和高敏C反应蛋白高表达的影响[J].中华实用诊断与治疗杂志,2009,23(11):1062-1064. 被引量:2
  • 10Berchner-Pfannschmidt U, Yamac H, Trinidad B, et al. Nitric oxide modulates oxygen sensing by hypoxia-inducible factor 1 dependent induction of prolyl hydroxylase 2[J]. J Biol Chem, 2007,282(3):1788-1796.

二级参考文献14

  • 1周燕.超敏C反应蛋白检测的临床意义[J].山西医药杂志,2006,35(10):917-918. 被引量:15
  • 2尹丽,李东野,夏勇.腺病毒介导HIF-1基因转染对心肌细胞缺血再灌注损伤的保护作用[J].国际心血管病杂志,2007,34(2):137-140. 被引量:4
  • 3Knikos A, Laherty C D, Dixit V M. Transcriptional actiration of the TNF-α inducible zinc finger protein 20, is mediated by kappa elements[J]. Biol Chem,1992,267(25) :1796-1977.
  • 4胡娟 王启军.肝癌患者组织中锌指蛋白216、A20mRNA表达与P53、P16基因表达缺失的相关性研究.临床实验室,2009,3(3):43-45.
  • 5Ohtani N, Yamakoshi K, Takahashi A, et al. The P16INR4a-Rb pathway: Molecular link hetweeular link[J]. J Med Invest,2004, 51(3-4) :146-153.
  • 6Ahmad T, Gore M. Review of the use of topotecen in ovanocn carcinoma[J]. Expert Opin Pharmacother, 2004,5(11):2333- 2340.
  • 7Patel V I, Daniel S, Longo C R, et al. A20, a modulator of smooth muscle cell proliferation and apoptosis, prevents and induces regression of neointimal hyperplasia[J]. FASEB J, 2006, 20(9) : 1418-1830.
  • 8Dixit V M, Green S, Sarma V, et al. Tumor necrosis factor- induction of novel genes in huanman endothelial a maerophage specific chemotaxin[J]. Biol Chem, 1990,265 (5) : 2973-2978.
  • 9Arvelo M B, Cooper J T, Long C, et al. A20 protects mice from D-galac-tosamine/lipopolysachride acute toxic lethal hepatitis[J]. Hepatology, 2002,35 (3) : 535-543.
  • 10Heyninck K, Beyaert R. A20 inhibits NF-kappa B activation by dual ubiquitin-editing functions[J]. Trends Biochem Sci,2005,30 (1):1-4.

共引文献9

同被引文献48

引证文献4

二级引证文献23

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部